The possibility of establishing a new method of treatment against pulmonary fibrosis caused by acute paraquat intoxication, which takes into consideration the role of heat shock protein 60 (HSP60), was investigated in paraquat-exposed rat lung mitochondria. In polyacrylamide electrophoresis, mitochondrial protein bands appeared, especially in the range of molecular weight 60 kDa and higher, whereas protein bands disappeared in the 20-40 kDa range on the 4th day after paraquat exposure. The protein profile was normalized on the 7th day and no remarkable changes were seen thereafter up to the 56th day. The changes seen during the observation period were thought to reflect the course of paraquat-induced dysfunction and subsequent repair. The malondialdehyde concentration in mitochondria decreased until the 7th day but subsequently increased and recovered to normal levels by the 56th day. The relative density of HSP60 increased until the 7th day but subsequently decreased and recovered to normal levels by the 56th day. These two parameters therefore showed symmetrical changes. The change in the malondialdehyde concentration was thought to reflect the course of activation of the antioxidation function in mitochondria and the progression of repair. The change in the relative density of HSP60 was thought to have increased to repair the proteins affected by the paraquat radical and to have normalized with the progression of healing. These results suggest that HSP60 may play an important role in preventing the progression of pulmonary fibrosis induced by paraquat.

No abstract